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| 1 | Immune therapy including dendritic cell based therapy in chronic hepatitis B virus infection显示文摘肝炎 B (HBV ) 感染是一个全球公共卫生问题。全球被感染了的约 20 亿个人,超过 4 亿是 HBV 的慢性带菌者。长期的 HBV 搬运人的可观的数字患进步的肝疾病。另外,所有 HBV 搬运人是这个病毒的永久来源。为长期的 HBV 搬运人没有药品治疗。然而,抗病毒的药为大约 10% 病人被推荐这些药是昂贵的,限制了功效,并且拥有可观的副作用。最近的研究证明了到 HBV 的主人的有免疫力的回答非常在长期的 HBV 感染的每个阶段被包含:(1 ) 这些影响长期的 HBV 带菌状态的获得,(2 ) 他们在肝损坏的上下文是重要的,(3 ) 从长期的 HBV 相关的肝疾病的恢复依赖于 HBV 特定的有免疫力的回答的自然和程度。然而,在长期的 HBV 搬运人的 HBV 特定的有免疫力的回答的足够的层次的正式就职是困难的。在最后一十年期间,肝炎 B 疫苗作为一条治疗学的途径(疫苗的治疗) 予长期的 HBV 搬运人被以。疫苗的治疗的现在的政体是安全、便宜,然而并非那么有效。一支树枝状的基于房间的治疗学的疫苗最近为治疗长期的 HBV 感染被开发了。在这评论,我们将为治疗长期的 HBV 感染包括疫苗的治疗和树枝状的基于房间的疫苗的治疗关于 HBV 特定的有免疫力的治疗的开发的概念,科学逻辑,策略和技术讨论。 | Sk Md Fazle Akbar Norio Horiike Morikazu Onji | 2006 | World Journal of Gastroenterology2006，12，18： | 35 |
| 2 | Prognosis following transcatheter arterial embolization for 121 patients with unresectable hepatocellular carcinoma with or without a history of treatment显示文摘瞄准:回顾地为 HCC 后面的 transcatheter 与肝细胞癌(HCC ) 评估病人的预后与或没有治疗的历史动脉的 embolization (TAE ) 。方法:有在我们的医院里从 1992 ~ 2004 与 TAE 对待的 HCC 的 121 个病人在这研究被注册。84 个病人为 HCC 有治疗的历史,当时 37。在入口,有额外肝的转移的病人,门静脉肿瘤血栓,或孩子呸班的时候, C 被排除。当 HCC 的复发被提高的肿瘤标记,或 ultrasonography 或动态计算断层摄影术调查结果诊断时, TAE 被重复。结果:肿瘤尺寸更大,没有过去的治疗(P<0.01 ) ,肿瘤的数字是在病人的少数。然而,在节点转移(TNM ) 舞台或幸存在 2 个组之间评估的肿瘤没有差别。一个双性人 alpha-fetoprotein (法新社)(>100 ng/mL ) 的小叶片的肿瘤和高水平是与在有 HCC 的历史的病人的差的预后有关的因素。结论:预后追随者 TAE 在有或没有过去的治疗的 HCC 病人之间是类似的。在到一堂重复 TAE 功课的入口能改进预后以前, HCC 或周期性的 HCC 和获得的好本地人的早诊断对 HCC 控制。 | Atsushi Hiraoka Teru Kumagi Masashi Hirooka Takahide Uehara Kiyotaka Kurose Hidehito luchi Yoichi Hiasa Bunzo Matsuura Kojiro Michitaka Seishi Kumano Hiroaki Tanaka Yoshimasa Yamashita Norio Horiike Teruhito Mochizuki Morikazu Onji | 2006 | World Journal of Gastroenterology2006，12，13： | 9 |
| 3 | Review:On dendritic cell-based therapy for cancers显示文摘Dendritic cells (DCs), the most prevalent antigen-presenting cell in vivo, had been widely characterized in the last three decades. DCs are present in almost all tissues of the body and play cardinal roles in recognition of microbial agents,autoantigens, allergens and alloantigen. DCs process the microbial agents or their antigens and migrate to lymphoid tissues to present the antigenic peptide to lymphocytes. This leads to activation of antigen-specific lymphocytes. Initially, it was assumed that DCs are principally involved in the induction and maintenance of adaptive immune responses, but now it is evident that DCs also have important roles in innate immunity. These features make DCs very good candidates for therapy against various pathological conditions including malignancies. Initially, DC-based therapy was used in animal models of cancers. Data from these studies inspired considerable optimism and DC-based therapies was started in human cancers 8 years ago. In general,DC-based therapy has been found to be safe in patients with cancers, although few controlled trials have been conducted in this regard. Because the fundamentals principles of human cancers and animal models of cancers are different, the therapeutic efficacy of the ongoing regime of DC-based therapy in cancer patients is not satisfactory. In this review, we covered the various aspects that should be considered for developing better regime of DC-based therapy for human cancers. | Morikazu Onji Sk.Md.Fazle Akbar | 2005 | Journal of Zhejiang University-Science B(Biomedicine & Biotechnology)2005，6，1： | 3 |
| 4 | Recurrence of autoimmune hepatitis after liver transplantation without elevation of alanine aminotransferase显示文摘It is controversial whether steroid therapy should be continued to prevent the recurrence of autoimmune hepatitis(AIH)in patients who have undergone liver transplantation(LTx)due to AIH.We report a case of recurrent autoimmune hepatitis after LTx despite a persistently normal range of alanine aminotransferase(ALT).A 50-year-old woman was admitted to our hospital because of jaundice and severe liver dysfunction,where she was diagnosed with liver failure due to AIH.Steroid therapy was not effective enough and the patient received living-donor LTx in 1999.Following the operation,the level of ALT was maintained within a normal range and anti-nuclear antibody(ANA)became negative,however,the serum level of IgG gradually elevated and ANA became positive,while platelets decreased.A liver biopsy performed 6 years after LTx showed histological findings of AIH and she was diagnosed with recurrent AIH.A recurrence of AIH may occur after LTx even if the level of ALT remains within a normal range.We consider that a protocol liver biopsy should be performed in patients who undergo LTx due to AIH to decide the indication for steroid therapy. | Huaiqi Yao Kojiro Michitaka Yoshio Tokumoto Yosuke Murata Toshie Mashiba Masanori Abe Yoichi Hiasa Norio Horiike Morikazu Onji | 2007 | World Journal of Gastroenterology2007，13，10： | 3 |
| 5 | Long‐term outcome of Japanese patients with type 1 autoimmune hepatitis显示文摘 | Kaname Yoshizawa Akihiro Matsumoto Tetsuya Ichijo Takeji Umemura Satoru Joshita Michiharu Komatsu Naoki Tanaka Eiji Tanaka Masao Ota Yoshihiko Katsuyama Kendo Kiyosawa Masanori Abe Morikazu Onji | 2012 | Hepatology2012，，： | 2 |
| 6 | Phase I/II study of immunotherapy using tumor antigen-pulsed dendriticcells in patients with hepatocellular carcinoma显示文摘 | Fujimasa Tada Masanori Abe Masashi Hirooka Yoshiou Ikeda Yoichi Hiasa Yoon Lee Nam-Chul Jung Woo-Bok Lee Hyun-Soo Lee Yong-Soo Bae Morikazu Onji | 2012 | International Journal of Oncology2012，，： | 2 |
| 7 | AIF-regulated oxidative phosphorylation supports lung cancer development显示文摘Cancer is a major and still increasing cause of death in humans. Most cancer cells have a fundamentally different metabolic profile from that of normal tissue. This shift away from mitochondrial ATP synthesis via oxidative phosphorylation towards a high rate of glycolysis, termed Warburg effect, has long been recognized as a paradigmatic hallmark of cancer, supporting the increased biosynthetic demands of tumor cells. Here we show that deletion of apoptosis-inducing factor (AIF) in a Kras^G12D-driven mouse lung cancer model resulted in a marked survival advantage, with delayed tumor onset and decreased malignant progression. Mechanistically, Aif deletion leads to oxidative phosphorylation (OXPHOS) deficiency and a switch in cellular metabolism towards glycolysis in non-transformed pneumocytes and at early stages of tumor development. Paradoxically, although Aif-deficient cells exhibited a metabolic Warburg profile, this bioenergetic change resulted in a growth disadvantage of Kras^G12D-driven as well as Kras wild-type lung cancer cells. Cell-autonomous re-expression of both wild-type and mutant AIF (displaying an intact mitochondrial, but abrogated apoptotic function) in Aif-knockout Kras^G12D mice restored OXPHOS and reduced animal survival to the same level as AIF wild-type mice. In patients with non-small cell lung cancer, high AIF expression was associated with poor prognosis. These data show that AIF-regulated mitochondrial respiration and OXPHOS drive the progression of lung cancer. | Shuan Rao Laura Mondragon Blanka Pranjic Toshikatsu Hanada Gautier Stoll Thomas Kocher Peng Zhang Alexander Jais Alexander Lercher Andreas Bergthaler Daniel Schramek Katharina Haigh Valentina Sica Marion Leduc Nazanine Modjtahedi Tsung-Pin Pai Masahiro Onji Iris Uribesalgo Reiko Hanada Ivona Kozieradzki Rubina Koglgruber Shane J. Cronin Zhigang She Franz Quehenberger Helmut Popper Lukas Kenner Jody J. Haigh Oliver Kepp Malgorzata Rak Kaican Cai Guido Kroemer Josef M. Penninger | 2019 | Cell Research2019，29，7： | 2 |
| 8 | Predictive values of amino acid sequences of the core and NS5A regions in antiviral therapy for hepatitis C: a Japanese multi-center study显示文摘 | Takeshi Okanoue Yoshito Itoh Hiroaki Hashimoto Kohichiroh Yasui Masahito Minami Tetsuo Takehara Eiji Tanaka Morikazu Onji Joji Toyota Kazuaki Chayama Kentaro Yoshioka Namiki Izumi Norio Akuta Hiromitsu Kumada | 2009 | Journal of Gastroenterology2009，，9： | 2 |
| 9 | Significance of study on prevalence of AMA in healthy subjects显示文摘 | Onji M Furukawa S | 2004 | Gastroenterol2004，39，： | 1 |
| 10 | Hepatitis B virus (HBV)-transgenic mice as an investigative tool to study immunopathology during HBV infection 显示文摘 | Akbar SK Onji M | 1998 | Int J Exp Pathol1998，79，： | 1 |
| 11 | The role of dysfunction of dendritic cells in hepatitis B virus persistent infection 显示文摘 | Horrike N Onji M | 2004 | Nippon Rinsho2004，628，： | 1 |
| 12 | Upregulation of II antigen on den dritic cells from hepatitis B virus transgenic mice by interferon-gamma: abrogat ion of immune response defect to a T-cell-dependent antigen显示文摘 | Akbar SM Inaba K Onji M | 1996 | Immunol ogy1996，87，4： | 1 |
| 13 | Intercellular adhesion molecule- 1 expression on the hepatocyle membrane of patients with chronic hepatitis B and C显示文摘 | Horiike N Onji M Kumon t | 1993 | Liver1993，13，1： | 1 |
| 14 | Presentation and diagnosis of primary biliary cirrhosis in the 21 st century显示文摘 | Kumagi T Onji M | 2008 | Clin Liver Dis2008，12，24： | 1 |
| 15 | Prognostic importance of antigen presenting dentritic cells during vaccine therapy in murine hepatitis B virus显示文摘 | HORIIK N ONJI M | 1999 | Immunology1999，6，4： | 1 |
| 16 | Serial observation of lymphocyte subpopulations and interleukin 2 production of T cells from patients with acute viral hepatitis and chronic active hepatitis显示文摘 | Onji M Kondo H Ohto Y | 1988 | Hepatogastroenterology1988，35，： | 1 |
| 17 | Clinical characteristics of drug-induced liver injury in the elderly 显示文摘 | Onji M Fujioka S Takeuchi Y eta1 | 2009 | Hepatol Res2009，39，6： | 1 |
| 18 | Intercellular adhesion molecule- 1 expression on the hepatocyte meo mbrane of patients with chronic hepatitis B and C 显示文摘 | Horiike N Onji M Kumon I | 1993 | Liver1993，13，： | 1 |
| 19 | Occurrence of ε-poly-L-lysine-degrading enzyme in ε-poly-L-lysine-tolerant Sphingobacterium multivorum OJ10: Purification and characterization 显示文摘 | Kito M Onji Y Yoshida T | 2002 | FEMS Microbiol Lett2002，207，2： | 1 |
| 20 | Guidelines for the treatment of chronic hepatitis and cirrhosis due to hepatitis C virus infection for the fiscal year 2008 in Japan显示文摘 | Kumada H Okanoue T Onji M | 2010 | Hepatol Res2010，40，1： | 1 |
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